The Journal of Cell Biology, Vol 101, 60-65, Copyright © 1985 by The Rockefeller University Press
Monensin-resistant mouse Balb/3T3 cell mutant with aberrant penetration of vesicular stomatitis virus
M Ono, K Mifune, A Yoshimura, S Ohnishi and M Kuwano
A mutant (MO-5) resistant to monensin (an ionophoric antibiotic) derived
from the mouse Balb/3T3 cell line, was a poor host for vesicular stomatitis
virus (VSV) or semliki forest virus (SFV) multiplication. The yield of VSV
particles in MO-5 is one 100-fold reduced as is VSV-dependent RNA
synthesis. In contrast to a pH-remedial mutant, the abortive production of
infectious VSV particles in MO-5 cells was not restored by low pH
treatment. The pH values in the endosome and the lysosome of MO-5 cells
were 5.2 and 5.4, respectively, values that were comparable to the pH value
in Balb/3T3 cells. Assays with [3H]uridine-labeled VSV indicated similar
binding of VSV in MO-5: percoll gradient centrifugation analysis of
[35S]methionine-labeled VSV- infected Balb/3T3 showed accumulation of VSV
in the lysosome fraction 20 min after VSV infection, whereas VSV can be
found mainly in endosome/Golgi fraction of MO-5 cells after 40 to 60 min on
the percoll gradients. Degradation of [35S]methionine-labeled VSV was
observed at a significant rate in Balb/3T3 cells, but not in MO-5 cells.
The monensin- resistant somatic cell may thus provide a genetic route to
study the mechanism of endocytosis or transport of enveloped viruses.
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